Normal sinus rhythm of the heart begins with the sinoatrial node (or “SA node”) generating a depolarization wave front, or electrical impulse. This impulse causes adjacent myocardial tissue cells in the right and left atria to depolarize. The electrical impulse uniformly propagates across the right and left atria and the atrial septum to the atrioventricular node (or “AV node”), causing the atria to contract and empty blood from the atria into the ventricles. The electrical impulse propagates through the AV node to the atrioventricular bundle (or “HIS bundle”), where it further propagates across the ventricles, causing the ventricles to contract. The AV node regulates the propagation delay to the HIS bundle, so that atrial systole occurs during ventricular diastole. This coordination of the electrical activity results in the described, organized sequence of myocardial contraction leading to a normal heartbeat.
Sometimes aberrant conductive pathways develop in heart tissue, which disrupt the normal path of depolarization events. For example, anatomical obstacles, called “conduction blocks,” can cause the electrical impulse to degenerate into several circular wavelets that circulate about the obstacles. These wavelets, called “reentry circuits,” disrupt the normal activation of the atria or ventricles. As a further example, localized regions of ischemic myocardial tissue may propagate depolarization events slower than normal myocardial tissue. The ischemic region, also called a “slow conduction zone,” creates errant, circular propagation patterns, called “circus motion.” The circus motion also disrupts the normal depolarization patterns, thereby disrupting the normal contraction of the heart tissue.
The aberrant conductive pathways create abnormal, irregular, and sometimes life-threatening heart rhythms, called arrhythmias. An arrhythmia can take place in the atria, for example, as in atrial tachycardia (AT) or atrial flutter (AF). The arrhythmia can also take place in the ventricle, for example, as in ventricular tachycardia (VT).
In treating arrhythmias, it is sometimes essential that the location of the sources of the aberrant pathways (called focal arrhythmia substrates) be located. Once located, the focal arrhythmia substrate can be destroyed, or ablated, e.g., by surgical cutting, or the application of heat. In particular, ablation can remove the aberrant conductive pathway, thereby restoring normal myocardial contraction. An example of such an ablation procedure is described in U.S. Pat. No. 5,471,982, issued to Edwards et al.
Alternatively, arrhythmias may be treated by actively interrupting all of the potential pathways for atrial reentry circuits by creating complex lesion patterns on the myocardial tissue. An example of such a procedure is described in U.S. Pat. No. 5,575,810, issued to Swanson et al.
Frequently, a focal arrhythmia substrate resides at the base, or within, one or more pulmonary veins, wherein the atrial tissue extends. The automaticity created by these substrates results in ectopic atrial tachycardia. Although the effect caused by the depolarization wavefront propagating from the pulmonary vein containing the substrate resembles that caused by multiple focal arrhythmia substrates within the atria, the atrial fibrillation is actually caused by a single focal arrhythmia substrate within the pulmonary vein. Arrhythmia substrates residing at the base of, or within, a pulmonary vein may alternatively originate from a re-entrant circuit with the depolarization wavefront propagating around a signal vein or within a slow conduction zone residing near or within the vein.
Current techniques of eradicating these substrates include steering a conventional ablation catheter within the target pulmonary vein and mapping this region to pinpoint the substrate. However, this is a time consuming and difficult process. Either extensive mapping must be performed within the pulmonary vein to accurately locate the target ablation site, or multiple lesions must be created to, in effect, “carpet bomb” the substrate. Moreover, the substrate may be located deep within the pulmonary vein, thereby making the manipulations required to steer the catheter's distal tip to the target site difficult.
Thus, it would be beneficial to provide more simplistic and efficient apparatus and methods for eradicating focal arrhythmia substrates residing at the base of, or within, a pulmonary vein.